Literature DB >> 20627827

Targeted eicosanoids lipidomics of exhaled breath condensate in healthy subjects.

Marek Sanak1, Anna Gielicz, Krzysztof Nagraba, Marek Kaszuba, Jagoda Kumik, Andrew Szczeklik.   

Abstract

BACKGROUND: Exhaled breath condensate collection is a non-invasive method of sampling the respiratory tract that can be repeated several times in a wide range of clinical settings. Quantitation of non-volatile compounds in the condensate requires highly sensitive analytical methods, e.g. mass spectrometry.
OBJECTIVE: To validate cross-platform measurements of eicosanoids using high performance liquid chromatography or gas chromatography coupled with mass spectrometry in exhaled breath condensate sampled from 58 healthy individuals.
METHODS: Twenty different eicosanoid compounds, representing major arachidonic acid lipoxygenation and cyclooxygenation pathways were measured using a stable isotope dilution method. We applied a free palmitic acid concentration as a surrogate marker for the condensate dilution factor.
RESULTS: Eicosanoids concentrations in the condensates were consistent with their content in other biological fluids. Prostaglandin E(2) was the most abundant mediator, represented by its stable metabolite tetranor-PGEM. Prostaglandin D(2) products were at low concentration, while hydroxyacids derived from lipoxygenation were abundant. 5-HETE was elevated in current tobacco smokers. Leukotriene B(4) has the highest concentration of all 5-LO products. 15-LO analogues of cysteinyl leukotrienes-eoxins were detectable and metabolized to eoxin E(4). Two main vascular prostanoids: prostacyclin and thromboxane B(2) were present as metabolites. A marker for non-enzymatic lipid peroxidation, 8-iso-PGF(2alpha) isoprostane was increased in smokers.
CONCLUSION: Presented targeted lipidomics analysis of exhaled breath condensate in healthy subjects justifies its application to investigation of inflammatory lung diseases. Measurements of non-volatile mediators of inflammation in the condensates might characterize disease-specific pathological mechanisms and responses to treatment.

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Year:  2010        PMID: 20627827     DOI: 10.1016/j.jchromb.2010.05.012

Source DB:  PubMed          Journal:  J Chromatogr B Analyt Technol Biomed Life Sci        ISSN: 1570-0232            Impact factor:   3.205


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